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Cirrhosis of the LiverCirrhosis of the Liver
Dr Ibraheem bashayreh, RN, PhD Dr Ibraheem bashayreh, RN, PhD
ANATOMY & PHYSIOLOGYANATOMY & PHYSIOLOGYLIVERa. Weighing between 1,200 and 1,600 g, the liver is the largest
glandular organ in the body. It is located in the right upper abdominal quadrant, under the right diaphragm.
b. The liver is divided into four lobes: left, right, caudate and quadrate. The lobes are further subdivided into smaller units known as lobules.
c. The liver contains several cell types including hepatocytes (ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that engulf bacteria).
d. Bile is continuously formed by hepatocytes (about 1L/day). Bile comprises water, electrolytes , lecithin,fatty acids, cholesterol, bilirubin and bile salts.
e. The Liver is surrounded by a tough fibroelastic capsule called Glisson’s capsule.
LIVERa. Weighing between 1,200 and 1,600 g, the liver is the largest
glandular organ in the body. It is located in the right upper abdominal quadrant, under the right diaphragm.
b. The liver is divided into four lobes: left, right, caudate and quadrate. The lobes are further subdivided into smaller units known as lobules.
c. The liver contains several cell types including hepatocytes (ie. Liver cells) and Kupffer cells (i.e. phagocytic cells that engulf bacteria).
d. Bile is continuously formed by hepatocytes (about 1L/day). Bile comprises water, electrolytes , lecithin,fatty acids, cholesterol, bilirubin and bile salts.
e. The Liver is surrounded by a tough fibroelastic capsule called Glisson’s capsule.
FUNCTIONS OF THE LIVERFUNCTIONS OF THE LIVER
• Regulating blood glucose level by making glycogen, which is stored in hepatocytes.
• Synthesizing blood glucose from amino acids of lactate through gluconeogenesis.
• Converting ammonia produced from gluconeogenetic by-products and bacteria to urea
• Synthesizing plasma proteins such as albumin, globulins, clotting factors, and lipoproteins.
• Breaking down fatty acids into ketone bodies• Storing vitamins and trace metals• Affecting drug metabolism and detoxification• Secreting bile
• Regulating blood glucose level by making glycogen, which is stored in hepatocytes.
• Synthesizing blood glucose from amino acids of lactate through gluconeogenesis.
• Converting ammonia produced from gluconeogenetic by-products and bacteria to urea
• Synthesizing plasma proteins such as albumin, globulins, clotting factors, and lipoproteins.
• Breaking down fatty acids into ketone bodies• Storing vitamins and trace metals• Affecting drug metabolism and detoxification• Secreting bile
Liver cirrhosis
DescriptionDescription
• A chronic, progressive disease of the liver
– Extensive parenchymal cell degeneration
– Destruction of parenchymal cells
• A chronic, progressive disease of the liver
– Extensive parenchymal cell degeneration
– Destruction of parenchymal cells
DescriptionDescription
• Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis
• Regenerative process is disorganized, resulting in abnormal blood vessel and bile duct relationships from fibrosis
DescriptionDescription
• Normal lobular structure distorted by fibrotic connective tissue
• Lobules are irregular in size and shape with impaired vascular flow
• Insidious, prolonged course
• Normal lobular structure distorted by fibrotic connective tissue
• Lobules are irregular in size and shape with impaired vascular flow
• Insidious, prolonged course
Etiology and PathophysiologyEtiology and Pathophysiology
• Cell necrosis occurs
• Destroyed liver cells are replaced by scar tissue
• Normal architecture becomes nodular
• Cell necrosis occurs
• Destroyed liver cells are replaced by scar tissue
• Normal architecture becomes nodular
Etiology and PathophysiologyEtiology and Pathophysiology
• Four types of cirrhosis:
– Alcoholic (Laennec’s) cirrhosis
– Postnecrotic cirrhosis
– Biliary cirrhosis
– Cardiac cirrhosis
• Four types of cirrhosis:
– Alcoholic (Laennec’s) cirrhosis
– Postnecrotic cirrhosis
– Biliary cirrhosis
– Cardiac cirrhosis
Etiology and PathophysiologyEtiology and Pathophysiology
• Alcoholic (Laennec’s) Cirrhosis
– Associated with alcohol abuse
– Preceded by a theoretically reversible fatty infiltration of the liver cells
– Widespread scar formation
• Alcoholic (Laennec’s) Cirrhosis
– Associated with alcohol abuse
– Preceded by a theoretically reversible fatty infiltration of the liver cells
– Widespread scar formation
Etiology and PathophysiologyEtiology and Pathophysiology
• Postnecrotic Cirrhosis
– Complication of toxic or viral hepatitis
– Accounts for 20% of the cases of cirrhosis
– Broad bands of scar tissue form within the liver
• Postnecrotic Cirrhosis
– Complication of toxic or viral hepatitis
– Accounts for 20% of the cases of cirrhosis
– Broad bands of scar tissue form within the liver
Etiology and PathophysiologyEtiology and Pathophysiology
• Biliary Cirrhosis – Associated with chronic biliary
obstruction and infection
– Accounts for 15% of all cases of cirrhosis
• Biliary Cirrhosis – Associated with chronic biliary
obstruction and infection
– Accounts for 15% of all cases of cirrhosis
Etiology and PathophysiologyEtiology and Pathophysiology
• Cardiac Cirrhosis – Results from longstanding severe
right-sided heart failure
• Cardiac Cirrhosis – Results from longstanding severe
right-sided heart failure
Manifestations of Liver CirrhosisManifestations of Liver Cirrhosis
Fig. 42-5
Clinical ManifestationsEarly Manifestations
Clinical ManifestationsEarly Manifestations
• Onset usually insidious
• GI disturbances:
– Anorexia
– Dyspepsia
– Flatulence
– N-V, change in bowel habits
• Onset usually insidious
• GI disturbances:
– Anorexia
– Dyspepsia
– Flatulence
– N-V, change in bowel habits
Clinical ManifestationsEarly Manifestations
Clinical ManifestationsEarly Manifestations
• Abdominal pain
• Fever
• Lassitude (laziness)
• Weight loss
• Enlarged liver or spleen
• Abdominal pain
• Fever
• Lassitude (laziness)
• Weight loss
• Enlarged liver or spleen
Clinical ManifestationsLate Manifestations
Clinical ManifestationsLate Manifestations
• Two causative mechanisms
– Hepatocellular failure
– Portal hypertension
• Two causative mechanisms
– Hepatocellular failure
– Portal hypertension
Clinical ManifestationsJaundice
Clinical ManifestationsJaundice
• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue
• Occurs because of insufficient conjugation of bilirubin by the liver cells, and local obstruction of biliary ducts by scarring and regenerating tissue
Clinical ManifestationsJaundice
Clinical ManifestationsJaundice
• Intermittent jaundice is characteristic of biliary cirrhosis
• Late stages of cirrhosis the patient will usually be jaundiced
• Intermittent jaundice is characteristic of biliary cirrhosis
• Late stages of cirrhosis the patient will usually be jaundiced
Clinical ManifestationsSkin
Clinical ManifestationsSkin
• Spider angiomas (telangiectasia, spider nevi)
• Palmar erythema
• Spider angiomas (telangiectasia, spider nevi)
• Palmar erythema
Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances
• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver
• Steroid hormones of the adrenal cortex (aldosterone), testes, and ovaries are metabolized and inactivated by the normal liver
Clinical Manifestations Endocrine DisturbancesClinical Manifestations Endocrine Disturbances
• Alteration in hair distribution
– Decreased amount of pubic hair
– Axillary and pectoral alopecia
• Alteration in hair distribution
– Decreased amount of pubic hair
– Axillary and pectoral alopecia
Clinical Manifestations Hematologic Disorders
Clinical Manifestations Hematologic Disorders
• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)
• Bleeding tendencies as a result of decreased production of hepatic clotting factors (II, VII, IX, and X)
Clinical Manifestations Hematologic Disorders
Clinical Manifestations Hematologic Disorders
• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism
• Anemia, leukopenia, and thrombocytopenia are believed to be result of hypersplenism
Clinical Manifestations Peripheral Neuropathy
Clinical Manifestations Peripheral Neuropathy
• Dietary deficiencies of thiamine, folic acid, and vitamin B12
• Dietary deficiencies of thiamine, folic acid, and vitamin B12
ComplicationsComplications
• Portal hypertension and esophageal varices • Peripheral edema and ascites• Hepatic encephalopathy• Fetor hepaticus: is bad breath with a 'dead
mouse' or sweet faecal smell. ... It may be caused by severe hepatocellular damage
• Portal hypertension and esophageal varices • Peripheral edema and ascites• Hepatic encephalopathy• Fetor hepaticus: is bad breath with a 'dead
mouse' or sweet faecal smell. ... It may be caused by severe hepatocellular damage
Complications Portal Hypertension
Complications Portal Hypertension
• Characterized by:
– Increased venous pressure in portal circulation
– Splenomegaly
– Esophageal varices
– Systemic hypertension
• Characterized by:
– Increased venous pressure in portal circulation
– Splenomegaly
– Esophageal varices
– Systemic hypertension
Complications Portal Hypertension
Complications Portal Hypertension
• Primary mechanism is the increased resistance to blood flow through the liver
• Primary mechanism is the increased resistance to blood flow through the liver
Complications Portal Hypertension
Splenomegaly
Complications Portal Hypertension
Splenomegaly
• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein
• Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the splenic vein
Complications Portal Hypertension Esophageal Varices
Complications Portal Hypertension Esophageal Varices
• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices
• Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus and produces varices
Complications Portal Hypertension Esophageal Varices
Complications Portal Hypertension Esophageal Varices
• Varices have fragile vessel walls which bleed easily
• Varices have fragile vessel walls which bleed easily
Complications Portal Hypertension
Internal Hemorrhoids
Complications Portal Hypertension
Internal Hemorrhoids
• Occurs because of the dilation of the mesenteric veins and rectal veins
• Occurs because of the dilation of the mesenteric veins and rectal veins
Complications Portal Hypertension
Caput Medusae
Complications Portal Hypertension
Caput Medusae
• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus
• Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins around the umbilicus
Complications Peripheral Edema and Ascites
Complications Peripheral Edema and Ascites
• Ascites:- - Intraperitoneal accumulation of
watery fluid containing small amounts of protein
• Ascites:- - Intraperitoneal accumulation of
watery fluid containing small amounts of protein
Complications Peripheral Edema and Ascites
Complications Peripheral Edema and Ascites
• Factors involved in the pathogenesis of ascites:
- Hypoalbuminemia Levels of aldosterone Portal hypertension
• Factors involved in the pathogenesis of ascites:
- Hypoalbuminemia Levels of aldosterone Portal hypertension
Complications Hepatic Encephalopathy
Complications Hepatic Encephalopathy
• Liver damage causes blood to enter systemic circulation without liver detoxification
• Liver damage causes blood to enter systemic circulation without liver detoxification
Complications Hepatic Encephalopathy
Complications Hepatic Encephalopathy
• Main pathogenic toxin is NH3 although other etiological factors have been identified
• Frequently a terminal complication
• Main pathogenic toxin is NH3 although other etiological factors have been identified
• Frequently a terminal complication
Complications Fetor HepaticusComplications Fetor Hepaticus
• Musty, sweetish odor detected on the patient’s breath
• From accumulation of digested by-products
• Musty, sweetish odor detected on the patient’s breath
• From accumulation of digested by-products
Development of AscitesDevelopment of Ascites
Fig. 42-6
Diagnostic StudiesDiagnostic Studies
• Liver function tests
• Liver biopsy
• Liver scan
• Liver ultrasound
• Liver function tests
• Liver biopsy
• Liver scan
• Liver ultrasound
Diagnostic StudiesDiagnostic Studies
• Esophagogastroduodenoscopy
• Prothrombin time
• Testing of stool for occult blood
• Esophagogastroduodenoscopy
• Prothrombin time
• Testing of stool for occult blood
Collaborative CareCollaborative Care
• Rest
• Avoidance of alcohol and anticoagulants
• Management of ascites
• Rest
• Avoidance of alcohol and anticoagulants
• Management of ascites
Collaborative CareCollaborative Care
• Prevention and management of esophageal variceal bleeding
• Management of encephalopathy
• Prevention and management of esophageal variceal bleeding
• Management of encephalopathy
Collaborative Care Ascites
Collaborative Care Ascites
• High carbohydrate, low protein, low Na+ diet
• Diuretics
• Paracentesis
• High carbohydrate, low protein, low Na+ diet
• Diuretics
• Paracentesis
Collaborative Care Ascites
Collaborative Care Ascites
• Peritoneovenous shunt
– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava
• Peritoneovenous shunt
– Provides for continuous reinfusion of ascitic fluid from the abdomen to the vena cava
Peritoneovenous ShuntPeritoneovenous Shunt
Fig. 42-8
Collaborative Care Esophageal Varices
Collaborative Care Esophageal Varices
• Avoid alcohol, aspirin, and irritating foods
• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)
• Avoid alcohol, aspirin, and irritating foods
• If bleeding occurs, stabilize patient and manage the airway, administer vasopressin (Pitressin)
Collaborative Care Esophageal Varices
Collaborative Care Esophageal Varices
• Endoscopic sclerotherapy or ligation
• Balloon tamponade
• Surgical shunting procedures (e.g., portacaval shunt, TIPS)
• Endoscopic sclerotherapy or ligation
• Balloon tamponade
• Surgical shunting procedures (e.g., portacaval shunt, TIPS)
Sengstaken-Blakemore TubeSengstaken-Blakemore Tube
Fig. 42-9
Portosystemic ShuntsPortosystemic Shunts
Fig. 42-11
Collaborative Care Hepatic EncephalopathyCollaborative Care
Hepatic Encephalopathy
• Goal: reduce NH3 formation– Protein restriction (0-40g/day)– Sterilization of GI tract with antibiotics
(e.g., neomycin)– lactulose (Cephulac) – traps NH3 in gut– levodopa
• Goal: reduce NH3 formation– Protein restriction (0-40g/day)– Sterilization of GI tract with antibiotics
(e.g., neomycin)– lactulose (Cephulac) – traps NH3 in gut– levodopa
Drug TherapyDrug Therapy
• There is no specific drug therapy for cirrhosis
• Drugs are used to treat symptoms and complications of advanced liver disease
• There is no specific drug therapy for cirrhosis
• Drugs are used to treat symptoms and complications of advanced liver disease
Nutritional TherapyNutritional Therapy
• Diet for patient without complications:
– High in calories CHO
– Moderate to low fat
– Amount of protein varies with degree of liver damage
• Diet for patient without complications:
– High in calories CHO
– Moderate to low fat
– Amount of protein varies with degree of liver damage
Nutritional TherapyNutritional Therapy
• Patient with hepatic encephalopathy
– Very low to no-protein diet
• Low sodium diet for patient with ascites and edema
• Patient with hepatic encephalopathy
– Very low to no-protein diet
• Low sodium diet for patient with ascites and edema
Nursing ManagementNursing Assessment
Nursing ManagementNursing Assessment
• Past health history
• Medications
• Chronic alcoholism
• Weight loss
• Past health history
• Medications
• Chronic alcoholism
• Weight loss
Nursing ManagementNursing Diagnoses
Nursing ManagementNursing Diagnoses
• Imbalanced nutrition: less than body requirements
• Impaired skin integrity• Ineffective breathing pattern• Risk for injury
• Imbalanced nutrition: less than body requirements
• Impaired skin integrity• Ineffective breathing pattern• Risk for injury
Nursing ManagementPlanning
Nursing ManagementPlanning
• Overall goals:
– Relief of discomfort
– Minimal to no complications
– Return to as normal a lifestyle as possible
• Overall goals:
– Relief of discomfort
– Minimal to no complications
– Return to as normal a lifestyle as possible
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
• Health Promotion
– Treat alcoholism
– Identify hepatitis early and treat
– Identify biliary disease early and treat
• Health Promotion
– Treat alcoholism
– Identify hepatitis early and treat
– Identify biliary disease early and treat
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition
• Acute Intervention– Rest– Edema and ascites– Paracentesis– Skin care– Dyspnea– Nutrition
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
• Acute Intervention
– Bleeding problems
– Balloon tamponade
– Altered body image
– Hepatic encephalopathy
• Acute Intervention
– Bleeding problems
– Balloon tamponade
– Altered body image
– Hepatic encephalopathy
Nursing ManagementNursing ImplementationNursing ManagementNursing Implementation
• Ambulatory and Home Care
– Symptoms of complications
– When to seek medical attention
– Remission maintenance
– Abstinence from alcohol
• Ambulatory and Home Care
– Symptoms of complications
– When to seek medical attention
– Remission maintenance
– Abstinence from alcohol
Nursing ManagementEvaluation
Nursing ManagementEvaluation
• Maintenance of normal body weight
• Maintenance of skin integrity
• Effective breathing pattern
• No injury
• No signs of infection
• Maintenance of normal body weight
• Maintenance of skin integrity
• Effective breathing pattern
• No injury
• No signs of infection
Gallbladder DisordersGallbladder DisordersGallbladder DisordersGallbladder Disorders
ANATOMY & PHYSIOLOGYANATOMY & PHYSIOLOGY
BILIARY SYSTEMa. Canaliculi – the smallest bile ducts located between
liver lobules, receive bile from hepatocytes. The canaliculi form larger bile ducts, which lead to hepatic duct.
b. Hepatic duct – from the liver joins the cystic duct from the gallbladder to form the common bile duct, which empties into the duodenum.
c. Sphincter of Oddi – controls the flow of bile into the intestine.
d. Gallbladder – is a hollow pear-shaped organ that is 30-40mm long. Normally holds 30-50mL of bile and can hold up to 70mL when fully distended.
BILIARY SYSTEMa. Canaliculi – the smallest bile ducts located between
liver lobules, receive bile from hepatocytes. The canaliculi form larger bile ducts, which lead to hepatic duct.
b. Hepatic duct – from the liver joins the cystic duct from the gallbladder to form the common bile duct, which empties into the duodenum.
c. Sphincter of Oddi – controls the flow of bile into the intestine.
d. Gallbladder – is a hollow pear-shaped organ that is 30-40mm long. Normally holds 30-50mL of bile and can hold up to 70mL when fully distended.
BILIARY SYSTEMBILIARY SYSTEM
• Draining bile from hepatocytes to the gallbladder by way of biliary tree
• Storing bile in the gallbladder and releasing it to the duodenum, which is mediated by the hormone cholecystokinin-pancreozymin.
• Draining bile from hepatocytes to the gallbladder by way of biliary tree
• Storing bile in the gallbladder and releasing it to the duodenum, which is mediated by the hormone cholecystokinin-pancreozymin.
The GallbladderThe Gallbladder
Located below the liver The cystic duct joins the hepatic duct to
become the bile ductThe common bile duct joins the pancreatic
duct in the sphincter of Oddi in the first part of the duodenum
Located below the liver The cystic duct joins the hepatic duct to
become the bile ductThe common bile duct joins the pancreatic
duct in the sphincter of Oddi in the first part of the duodenum
Stores and concentrates bileContracts during the digestion of fats to
deliver the bileCholecystokinin is released by the duodenal
cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi
Stores and concentrates bileContracts during the digestion of fats to
deliver the bileCholecystokinin is released by the duodenal
cells, causing the contraction of the gallbladder and relaxation of the sphincter of Oddi
CHOLELITHIASISCHOLELITHIASIS
• Refers to formation of calculi (ie, gallstones in the bladder.
• Predisposing Factors:1. Obese2. Female3. >40 yrs4. OC, Estrogen, intake5. Fair
• Refers to formation of calculi (ie, gallstones in the bladder.
• Predisposing Factors:1. Obese2. Female3. >40 yrs4. OC, Estrogen, intake5. Fair
CHOLELITHIASISCHOLELITHIASISSupersaturated bile, Biliary stasis
Stone formation
Blockage of Gallbladder
Inflammation, Mucosal Damage and WBC infiltration
CHOLECYSTITIS
Common locations of gallstonesCommon locations of gallstones
Gall StonesGall Stones
CHOLECYSTITISCHOLECYSTITIS
– inflammation of gallbladder with gallstone formation.
– inflammation of gallbladder with gallstone formation.
PATHOLOGY-SIGNS AND SYMPTOMS
CHOLECYSTITIS/ CHOLELITHIASISCHOLECYSTITIS/ CHOLELITHIASIS
Signs and Symptoms:• Severe Right abdominal pain radiating to the
back• Fever• Fat intolerance• Anorexia, n/v• Jaundice• Pruritus• Easy bruising • Tea colored urine• Steatorrhea
Signs and Symptoms:• Severe Right abdominal pain radiating to the
back• Fever• Fat intolerance• Anorexia, n/v• Jaundice• Pruritus• Easy bruising • Tea colored urine• Steatorrhea
CHOLECYSTITIS/ CHOLELITHIASISCHOLECYSTITIS/ CHOLELITHIASIS
Diagnosis:
• US detects the presence of gallstone
• Serum alkaline phosphatase – 50-120 u/L
• WBC
• Endoscopic retrograde cholangiopancreatography (ERCP) -
Diagnosis:
• US detects the presence of gallstone
• Serum alkaline phosphatase – 50-120 u/L
• WBC
• Endoscopic retrograde cholangiopancreatography (ERCP) -
CHOLECYSTITIS/ CHOLELITHIASISCHOLECYSTITIS/ CHOLELITHIASISNursing Management:• Administer Rx Medications • Diet – increase CHO, moderate CHON,
decrease fats • Meticulous skin care• Instruct patient to AVOID HIGH- fat diet and
GAS-forming foods• Assist in surgical and non-surgical measures• ESWL – non-invasive fragmentation of stones
by using repeated shockwaves directed at the gallstones in the gallbladder or common bile duct.
Nursing Management:• Administer Rx Medications • Diet – increase CHO, moderate CHON,
decrease fats • Meticulous skin care• Instruct patient to AVOID HIGH- fat diet and
GAS-forming foods• Assist in surgical and non-surgical measures• ESWL – non-invasive fragmentation of stones
by using repeated shockwaves directed at the gallstones in the gallbladder or common bile duct.
CHOLELITHIASIS/CHOLECYSTITIS
CHOLELITHIASIS/CHOLECYSTITIS
• Surgical procedures- Surgical Cholecystectomy, Choledochotomy,
• Laparoscopic cholecystectomy
• Surgical procedures- Surgical Cholecystectomy, Choledochotomy,
• Laparoscopic cholecystectomy
CHOLELITHIASIS/CHOLECYSTITIS
CHOLELITHIASIS/CHOLECYSTITIS
Post-operative nursing interventions
1. Monitor for surgical complications2. Post-operative position after recovery from
anesthesia- LOW FOWLER’s3. Encourage early ambulation 4. Administer medication before coughing and
deep breathing exercises5. Advise client to splint the abdomen to prevent
discomfort during coughing6. Administer analgesics, antiemetics, antacids7. Care of the biliary drainageor T-tube drainage8. Fat restriction is only limited to 4-6 weeks.
Normal diet is resumed
Post-operative nursing interventions
1. Monitor for surgical complications2. Post-operative position after recovery from
anesthesia- LOW FOWLER’s3. Encourage early ambulation 4. Administer medication before coughing and
deep breathing exercises5. Advise client to splint the abdomen to prevent
discomfort during coughing6. Administer analgesics, antiemetics, antacids7. Care of the biliary drainageor T-tube drainage8. Fat restriction is only limited to 4-6 weeks.
Normal diet is resumed